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Article: S RNA Intergenic Deletions Drive Viral Interference during Arenavirus Infections.

Hackbart, Matthew / López, Carolina B

bioRxiv : the preprint server for biology

2023

Abstract: Arenaviruses, a family of negative-sense RNA viruses spread by rodents, are a leading cause of severe hemorrhagic fever in humans. Due to a paucity of antivirals and vaccines for arenaviruses, there is a need to identify new mechanisms for interfering ... ...

Abstract	Arenaviruses, a family of negative-sense RNA viruses spread by rodents, are a leading cause of severe hemorrhagic fever in humans. Due to a paucity of antivirals and vaccines for arenaviruses, there is a need to identify new mechanisms for interfering with arenavirus replication. In several negative-sense RNA viruses, natural viral interference results from the production of non-standard viral genomes (nsVGs) that activate the innate immune system and/or compete for essential viral products. Although it is well established that arenaviruses produce strong interfering activities, it is unknown if they produce interfering nsVGs. Here we show that arenaviruses produce deletions within the intergenic region of their Small (S) RNA genome, which prevents the production of viral mRNA and protein. These deletions are more abundant when arenaviruses are grown in high-interfering conditions and are associated with inhibited viral replication. Overall, we found that arenaviruses produce internal deletions within the S RNA intergenic region that are produced by arenaviruses and can block viral replication. These natural arenavirus interfering molecules provide a new target for the generation of antivirals as well as an alternative strategy for producing attenuated arenaviruses for vaccines.
Language	English
Publishing date	2023-11-01
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.10.31.564889
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Article ; Online: Copy-back viral genomes induce a cellular stress response that interferes with viral protein expression without affecting antiviral immunity.

González Aparicio, Lavinia J / Yang, Yanling / Hackbart, Matthew / López, Carolina B

PLoS biology

2023 Volume 21, Issue 11, Page(s) e3002381

Abstract: Antiviral responses are often accompanied by translation inhibition and formation of stress granules (SGs) in infected cells. However, the triggers for these processes and their role during infection remain subjects of active investigation. Copy-back ... ...

Abstract	Antiviral responses are often accompanied by translation inhibition and formation of stress granules (SGs) in infected cells. However, the triggers for these processes and their role during infection remain subjects of active investigation. Copy-back viral genomes (cbVGs) are the primary inducers of the mitochondrial antiviral signaling (MAVS) pathway and antiviral immunity during Sendai virus (SeV) and respiratory syncytial virus (RSV) infections. The relationship between cbVGs and cellular stress during viral infections is unknown. Here, we show that SGs form during infections containing high levels of cbVGs, and not during infections with low levels of cbVGs. Moreover, using RNA fluorescent in situ hybridization to differentiate accumulation of standard viral genomes from cbVGs at a single-cell level during infection, we show that SGs form exclusively in cells that accumulate high levels of cbVGs. Protein kinase R (PKR) activation is increased during high cbVG infections and, as expected, is necessary for virus-induced SGs. However, SGs form independent of MAVS signaling, demonstrating that cbVGs induce antiviral immunity and SG formation through 2 independent mechanisms. Furthermore, we show that translation inhibition and SG formation do not affect the overall expression of interferon and interferon stimulated genes during infection, making the stress response dispensable for global antiviral immunity. Using live-cell imaging, we show that SG formation is highly dynamic and correlates with a drastic reduction of viral protein expression even in cells infected for several days. Through analysis of active protein translation at a single-cell level, we show that infected cells that form SGs show inhibition of protein translation. Together, our data reveal a new cbVG-driven mechanism of viral interference where cbVGs induce PKR-mediated translation inhibition and SG formation, leading to a reduction in viral protein expression without altering overall antiviral immunity.
MeSH term(s)	Humans ; Viral Proteins/genetics ; Viral Proteins/metabolism ; In Situ Hybridization, Fluorescence ; Interferons/metabolism ; Protein Biosynthesis ; Genome, Viral ; Cytoplasmic Granules/metabolism ; Virus Replication/genetics
Chemical Substances	Viral Proteins ; Interferons (9008-11-1)
Language	English
Publishing date	2023-11-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.3002381
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Article: VODKA2: A fast and accurate method to detect non-standard viral genomes from large RNA-seq datasets.

Achouri, Emna / Felt, Sébastien A / Hackbart, Matthew / Rivera-Espinal, Nicole S / López, Carolina B

bioRxiv : the preprint server for biology

2023

Abstract: During viral replication, viruses carrying an RNA genome produce non-standard viral genomes (nsVGs), including copy-back viral genomes (cbVGs) and deletion viral genomes (delVGs), that play a crucial role in regulating viral replication and pathogenesis. ...

Abstract	During viral replication, viruses carrying an RNA genome produce non-standard viral genomes (nsVGs), including copy-back viral genomes (cbVGs) and deletion viral genomes (delVGs), that play a crucial role in regulating viral replication and pathogenesis. Because of their critical roles in determining the outcome of RNA virus infections, the study of nsVGs has flourished in recent years exposing a need for bioinformatic tools that can accurately identify them within Next-Generation Sequencing data obtained from infected samples. Here, we present our data analysis pipeline, Viral Opensource DVG Key Algorithm2 (VODKA2), that is optimized to run on a High Performance Computing (HPC) environment for fast and accurate detection of nsVGs from large data sets.
Language	English
Publishing date	2023-07-15
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.04.25.537842
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Article ; Online: VODKA2: a fast and accurate method to detect non-standard viral genomes from large RNA-seq data sets.

Achouri, Emna / Felt, Sébastien A / Hackbart, Matthew / Rivera-Espinal, Nicole S / López, Carolina B

RNA (New York, N.Y.)

2023 Volume 30, Issue 1, Page(s) 16–25

Abstract	During viral replication, viruses carrying an RNA genome produce non-standard viral genomes (nsVGs), including copy-back viral genomes (cbVGs) and deletion viral genomes (delVGs), that play a crucial role in regulating viral replication and pathogenesis. Because of their critical roles in determining the outcome of RNA virus infections, the study of nsVGs has flourished in recent years, exposing a need for bioinformatic tools that can accurately identify them within next-generation sequencing data obtained from infected samples. Here, we present our data analysis pipeline, Viral Opensource DVG Key Algorithm 2 (VODKA2), that is optimized to run on a parallel computing environment for fast and accurate detection of nsVGs from large data sets.
MeSH term(s)	RNA-Seq ; Genome, Viral ; Algorithms ; Computational Biology/methods ; Virus Replication ; RNA, Viral/genetics
Chemical Substances	RNA, Viral
Language	English
Publishing date	2023-12-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	1241540-6
ISSN	1469-9001 ; 1355-8382
ISSN (online)	1469-9001
ISSN	1355-8382
DOI	10.1261/rna.079747.123
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Zs.A 4777: Show issues

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Article: Copy-back viral genomes induce a cellular stress response that interferes with viral protein expression without affecting antiviral immunity.

Lopez, Carolina B / Gonzalez Aparicio, Lavinia J / Yang, Yanling / Hackbart, Matthew S

bioRxiv : the preprint server for biology

2023

Abstract: Antiviral responses are often accompanied by translation inhibition and formation of stress granules (SG) in infected cells. However, the triggers for these processes and their role during infection remain subjects of active investigation. Copy-back ... ...

Abstract	Antiviral responses are often accompanied by translation inhibition and formation of stress granules (SG) in infected cells. However, the triggers for these processes and their role during infection remain subjects of active investigation. Copy-back viral genomes (cbVGs) are the primary inducers of the Mitochondrial Antiviral Signaling (MAVS) pathway and antiviral immunity during Sendai Virus (SeV) and Respiratory Syncytial virus (RSV) infections. The relationship between cbVGs and cellular stress during viral infections is unknown. Here we show that SG form during infections containing high levels of cbVGs, and not during infections with low levels of cbVGs. Moreover, using RNA fluorescent in situ hybridization to differentiate accumulation of standard viral genomes from cbVGs at a single-cell level during infection, we show that SG form exclusively in cells that accumulate high levels of cbVGs. PKR activation is increased during high cbVG infections and, as expected, PKR is necessary to induce virus-induced SG. However, SG form independent of MAVS signaling, demonstrating that cbVGs induce antiviral immunity and SG formation through two independent mechanisms. Furthermore, we show that translation inhibition and SG formation do not affect the overall expression of interferon and interferon stimulated genes during infection, making the stress response dispensable for antiviral immunity. Using live-cell imaging, we show that SG formation is highly dynamic and correlates with a drastic reduction of viral protein expression even in cells infected for several days. Through analysis of active protein translation at a single cell level, we show that infected cells that form SG show inhibition of protein translation. Together, our data reveal a new cbVG-driven mechanism of viral interference where cbVGs induce PKR-mediated translation inhibition and SG formation leading to a reduction in viral protein expression without altering overall antiviral immunity.
Language	English
Publishing date	2023-08-07
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.17.541157
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Coronavirus endoribonuclease targets viral polyuridine sequences to evade activating host sensors.

Hackbart, Matthew / Deng, Xufang / Baker, Susan C

Proceedings of the National Academy of Sciences of the United States of America

2020 Volume 117, Issue 14, Page(s) 8094–8103

Abstract: Coronaviruses (CoVs) are positive-sense RNA viruses that can emerge from endemic reservoirs and infect zoonotically, causing significant morbidity and mortality. CoVs encode an endoribonuclease designated EndoU that facilitates evasion of host pattern ... ...

Abstract	Coronaviruses (CoVs) are positive-sense RNA viruses that can emerge from endemic reservoirs and infect zoonotically, causing significant morbidity and mortality. CoVs encode an endoribonuclease designated EndoU that facilitates evasion of host pattern recognition receptor MDA5, but the target of EndoU activity was not known. Here, we report that EndoU cleaves the 5'-polyuridines from negative-sense viral RNA, termed PUN RNA, which is the product of polyA-templated RNA synthesis. Using a virus containing an EndoU catalytic-inactive mutation, we detected a higher abundance of PUN RNA in the cytoplasm compared to wild-type-infected cells. Furthermore, we found that transfecting PUN RNA into cells stimulates a robust, MDA5-dependent interferon response, and that removal of the polyuridine extension on the RNA dampens the response. Overall, the results of this study reveal the PUN RNA to be a CoV MDA5-dependent pathogen-associated molecular pattern (PAMP). We also establish a mechanism for EndoU activity to cleave and limit the accumulation of this PAMP. Since EndoU activity is highly conserved in all CoVs, inhibiting this activity may serve as an approach for therapeutic interventions against existing and emerging CoV infections.
MeSH term(s)	Animals ; Antiviral Agents/pharmacology ; Cell Line ; Chlorocebus aethiops ; Coronavirus/enzymology ; Coronavirus/immunology ; Coronavirus/metabolism ; Coronavirus Infections/immunology ; Coronavirus Infections/virology ; Endoribonucleases/genetics ; Endoribonucleases/metabolism ; Host Microbial Interactions/physiology ; Humans ; Interferons/pharmacology ; Poly U/chemistry ; Poly U/metabolism ; RNA, Viral/genetics ; RNA, Viral/metabolism ; Uridine/chemistry ; Vero Cells ; Viral Nonstructural Proteins/genetics ; Viral Nonstructural Proteins/metabolism ; Virus Replication/physiology
Chemical Substances	Antiviral Agents ; RNA, Viral ; Viral Nonstructural Proteins ; Poly U (27416-86-0) ; Interferons (9008-11-1) ; Endoribonucleases (EC 3.1.-) ; nidoviral uridylate-specific endoribonuclease (EC 3.1.-) ; Uridine (WHI7HQ7H85)
Keywords	covid19
Language	English
Publishing date	2020-03-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1921485117
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Zs.A 1148: Show issues

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Article ; Online: Copy-back viral genomes induce a cellular stress response that interferes with viral protein expression without affecting antiviral immunity.

Lavinia J González Aparicio / Yanling Yang / Matthew Hackbart / Carolina B López

PLoS Biology, Vol 21, Iss 11, p e

2023 Volume 3002381

Abstract	Antiviral responses are often accompanied by translation inhibition and formation of stress granules (SGs) in infected cells. However, the triggers for these processes and their role during infection remain subjects of active investigation. Copy-back viral genomes (cbVGs) are the primary inducers of the mitochondrial antiviral signaling (MAVS) pathway and antiviral immunity during Sendai virus (SeV) and respiratory syncytial virus (RSV) infections. The relationship between cbVGs and cellular stress during viral infections is unknown. Here, we show that SGs form during infections containing high levels of cbVGs, and not during infections with low levels of cbVGs. Moreover, using RNA fluorescent in situ hybridization to differentiate accumulation of standard viral genomes from cbVGs at a single-cell level during infection, we show that SGs form exclusively in cells that accumulate high levels of cbVGs. Protein kinase R (PKR) activation is increased during high cbVG infections and, as expected, is necessary for virus-induced SGs. However, SGs form independent of MAVS signaling, demonstrating that cbVGs induce antiviral immunity and SG formation through 2 independent mechanisms. Furthermore, we show that translation inhibition and SG formation do not affect the overall expression of interferon and interferon stimulated genes during infection, making the stress response dispensable for global antiviral immunity. Using live-cell imaging, we show that SG formation is highly dynamic and correlates with a drastic reduction of viral protein expression even in cells infected for several days. Through analysis of active protein translation at a single-cell level, we show that infected cells that form SGs show inhibition of protein translation. Together, our data reveal a new cbVG-driven mechanism of viral interference where cbVGs induce PKR-mediated translation inhibition and SG formation, leading to a reduction in viral protein expression without altering overall antiviral immunity.
Keywords	Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2023-11-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Coronavirus endoribonuclease targets viral polyuridine sequences to evade activating host sensors

Hackbart, Matthew / Deng, Xufang / Baker, Susan C

Proc Natl Acad Sci U S A

Abstract	Coronaviruses (CoVs) are positive-sense RNA viruses that can emerge from endemic reservoirs and infect zoonotically, causing significant morbidity and mortality. CoVs encode an endoribonuclease designated EndoU that facilitates evasion of host pattern recognition receptor MDA5, but the target of EndoU activity was not known. Here, we report that EndoU cleaves the 5'-polyuridines from negative-sense viral RNA, termed PUN RNA, which is the product of polyA-templated RNA synthesis. Using a virus containing an EndoU catalytic-inactive mutation, we detected a higher abundance of PUN RNA in the cytoplasm compared to wild-type-infected cells. Furthermore, we found that transfecting PUN RNA into cells stimulates a robust, MDA5-dependent interferon response, and that removal of the polyuridine extension on the RNA dampens the response. Overall, the results of this study reveal the PUN RNA to be a CoV MDA5-dependent pathogen-associated molecular pattern (PAMP). We also establish a mechanism for EndoU activity to cleave and limit the accumulation of this PAMP. Since EndoU activity is highly conserved in all CoVs, inhibiting this activity may serve as an approach for therapeutic interventions against existing and emerging CoV infections.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #11430
Database	COVID19

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Article ; Online: Detecting SARS-CoV-2 3CLpro expression and activity using a polyclonal antiserum and a luciferase-based biosensor.

O'Brien, Amornrat / Chen, Da-Yuan / Hackbart, Matthew / Close, Brianna J / O'Brien, Timothy E / Saeed, Mohsan / Baker, Susan C

Virology

2021 Volume 556, Page(s) 73–78

Abstract: The need to stem the current outbreak of SARS-CoV-2 responsible for COVID-19 is driving the search for inhibitors that will block coronavirus replication and pathogenesis. The coronavirus 3C-like protease (3CLpro) encoded in the replicase polyprotein is ... ...

Abstract	The need to stem the current outbreak of SARS-CoV-2 responsible for COVID-19 is driving the search for inhibitors that will block coronavirus replication and pathogenesis. The coronavirus 3C-like protease (3CLpro) encoded in the replicase polyprotein is an attractive target for antiviral drug development because protease activity is required for generating a functional replication complex. Reagents that can be used to screen for protease inhibitors and for identifying the replicase products of SARS-CoV-2 are urgently needed. Here we describe a luminescence-based biosensor assay for evaluating small molecule inhibitors of SARS-CoV-2 3CLpro/main protease. We also document that a polyclonal rabbit antiserum developed against SARS-CoV 3CLpro cross reacts with the highly conserved 3CLpro of SARS-CoV-2. These reagents will facilitate the pre-clinical evaluation of SARS-CoV-2 protease inhibitors.
MeSH term(s)	Animals ; Antiviral Agents/pharmacology ; Biosensing Techniques/methods ; Coronavirus 3C Proteases/antagonists & inhibitors ; Coronavirus 3C Proteases/genetics ; Coronavirus 3C Proteases/immunology ; Coronavirus 3C Proteases/metabolism ; Cross Reactions ; Immune Sera/immunology ; Luciferases/genetics ; Luciferases/metabolism ; Protease Inhibitors/pharmacology ; Rabbits ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/metabolism ; SARS Virus/immunology ; SARS Virus/metabolism ; SARS-CoV-2/drug effects ; SARS-CoV-2/genetics ; SARS-CoV-2/immunology ; SARS-CoV-2/metabolism ; Viral Nonstructural Proteins/genetics ; Viral Nonstructural Proteins/immunology ; Viral Nonstructural Proteins/metabolism ; Virus Replication/drug effects
Chemical Substances	Antiviral Agents ; Immune Sera ; Protease Inhibitors ; Recombinant Fusion Proteins ; Viral Nonstructural Proteins ; Luciferases (EC 1.13.12.-) ; 3C-like proteinase, SARS-CoV-2 (EC 3.4.22.-) ; Coronavirus 3C Proteases (EC 3.4.22.28)
Language	English
Publishing date	2021-01-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2021.01.010
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Article ; Online: Coronavirus Endoribonuclease and Deubiquitinating Interferon Antagonists Differentially Modulate the Host Response during Replication in Macrophages.

Volk, Aaron / Hackbart, Matthew / Deng, Xufang / Cruz-Pulido, Yazmin / O'Brien, Amornrat / Baker, Susan C

Journal of virology

2020 Volume 94, Issue 11

Abstract: Coronaviruses (CoVs) encode multiple interferon (IFN) antagonists that modulate the host response to virus replication. Here, we evaluated the host transcriptional response to infection with murine coronaviruses encoding independent mutations in one of ... ...

Abstract	Coronaviruses (CoVs) encode multiple interferon (IFN) antagonists that modulate the host response to virus replication. Here, we evaluated the host transcriptional response to infection with murine coronaviruses encoding independent mutations in one of two different viral antagonists, the deubiquitinase (DUB) within nonstructural protein 3 or the endoribonuclease (EndoU) within nonstructural protein 15. We used transcriptomics approaches to compare the scope and kinetics of the host response to the wild-type (WT), DUBmut, and EndoUmut viruses in infected macrophages. We found that the EndoUmut virus activates a focused response that predominantly involves type I interferons and interferon-related genes, whereas the WT and DUBmut viruses more broadly stimulate upregulation of over 2,800 genes, including networks associated with activating the unfolded protein response (UPR) and the proinflammatory response associated with viral pathogenesis. This study highlights the role of viral interferon antagonists in shaping the kinetics and magnitude of the host response during virus infection and demonstrates that inactivating a dominant viral antagonist, the coronavirus endoribonuclease, dramatically alters the host response in macrophages.
MeSH term(s)	Animals ; Computational Biology ; Coronavirus/physiology ; Coronavirus Infections/genetics ; Coronavirus Infections/immunology ; Coronavirus Infections/metabolism ; Coronavirus Infections/virology ; Cytokines/metabolism ; Endoribonucleases/metabolism ; Gene Expression Profiling ; Host-Pathogen Interactions/genetics ; Host-Pathogen Interactions/immunology ; Inflammation Mediators/metabolism ; Interferons/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/virology ; Mice ; Models, Biological ; Mutation ; RNA, Viral ; Unfolded Protein Response ; Viral Nonstructural Proteins/metabolism ; Virus Replication
Chemical Substances	Cytokines ; Inflammation Mediators ; RNA, Viral ; Viral Nonstructural Proteins ; Interferons (9008-11-1) ; Endoribonucleases (EC 3.1.-)
Keywords	covid19
Language	English
Publishing date	2020-05-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.00178-20
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